pharm 2 Flashcards

1
Q

moa of propofol

A

direct gaba a agonist-> increased cl conductance-> neuronal hyperpolarization

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2
Q

doa of propofol

A

5-10 mins

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3
Q

clearance of propofol

A

liver (p450) and extrahepatic metabolism (lungs)

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4
Q

which way does co2 response curve get shifted with propofol

A

down and to R (less sensitive to co2)

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5
Q

what does propofol do to hypoxic ventilatory drive

A

inhibits it

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6
Q

does propofol effect myocardial contractility

A

decreases it

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7
Q

does propofol effect venous tone

A

yes- decreased preload

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8
Q

cns effects of propofol

A

no analgesia!

dec cbf, icp, iop, cmro2

anticonvulsant properties

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9
Q

what is propofol made of

A

egg lecithin, soybean oil, glycerol

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10
Q

what allergy is a concern with propofol

A

egg allergy is fine - egg lecithin comes from the yolk- most egg allergy is to albumin in egg white

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11
Q

propofol infusion syndrome risk factors

A

-propofol dose > 4 mg/kg/hr
-propofol infusion duration >48 hrs
-adults > children
-inadequate oxygen delivery
-sepsis
-significant cerebral injury

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12
Q

clinical presentation of propofol infusion syndrome

A

-acute refractory bradycardia -> asystole

+
-metabolic acidosis
-rhabdo
-enlarged/ fatty liver
-renal failure
-HLD
-lipemia (cloudy plasma or blood)

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13
Q

how long is a propofol syrnige good for

A

6 hrs

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14
Q

how long is prop infusion good for

A

12 hrs

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15
Q

what preservatives are in propofol

A

diprivan contains edta

generic propofol- different preservatives- metabisulfite - bronchospasm; benzyl alcohol in infants

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16
Q

propofol injection pain can be minimized/ eliminated by

A

-injecting into lg more proximal vein
-lidocaine (before or mixed)
-opioid before propofol

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17
Q

what amount of propofol is used for ponv

A

10-20 mg IV

infusion: 10 mcg/kg/min

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18
Q

fospropofol

A

prodrug, propofol is active metabolite

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19
Q

what converts fospropofol to propofol

A

alkaline phosphatase

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20
Q

how does ketamine work

A

nmda antagonist (antagonizes glutamate)

seconday receptor targets opioid, MAO, serotonin, NE, muscarinic, na channels

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21
Q

what does ketamine dissociate

A

thalmus (sensory) from limbic system (awareness)

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22
Q

induction dose for ketamine

A

1-2 mg/kg

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23
Q

im ketamine dose

A

4-8 mg/kg

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24
Q

ketamine onset

A

iv 30-60 sec
im 2-4 min

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25
duration of ketamine
10-20 min (may require 60-90 min for full orientation)
26
clearance for keramine
liver (p450 enzymes)
27
does ketamine make matabolizes
yes active metabolite: norketamine (1/3-1/5 potency of ketamine)
28
what does chronic ketamine use do
induces liver enzymes (burn patients)
29
when would increased SNS from ketamine be harmful
severe CAD usually subhypnotic doses < 0.5 mg/kg usually doesnt activate SNS
30
myocardial effects of ketamine
myocardial depressant!! it only increases CO, HR< SVR< PVR if you have intact SNS - depressant effects unmasked if pt has depleted catecholamine (sepsis) or sympathectomy
31
what pt do you need to be careful about the pvr effects of ketamine with
severe rv failure- causes increased pvr
32
respiratory effects of ketamine
-bronchodilation (great choice if pt is actively wheezing) -upper airway muscle tone and airway reflexes remain intact -does not significantly shift co2 response curve -increased oral and pulmonary secretions- increased risk of laryngospasm
33
cns effects
increased cmro2, cbf, icp, eeg, nystagmus, emergence delirium
34
emergence delirium what is it and how to prevent
-presents as nightmares and hallucinations (risk for up to 24 hours) -benzos are most effective way to prevent emergent delirium (versed > diazepam)
35
risks for emergence delirium
age > 15 yrs, female, ketamine > 2 mg/kg, hx of personality disorder
36
ketamine analgesia properties
-good analgesia and opioid sparing effect (only induction agent that does this) -somatic pain > visceral pain -blocks central sensitization and wind up in dorsal horn of spinal cord -prevents opioid induced hyperalgesia (after remifentinal infusion) -excellent for burn patients and those with pre existing chronic pain syndromes
37
duration of etomidate
5-15 min
38
etomidate clearance
hepatic p450 enzymes and plasma esterases
39
cv effects
-minimal change in HR, SV or CO -SVR decreased- small reduction in bp -does not block sns response to laryngoscopy- give esmolol or opioid mild resp depression (less than versed or prop)
40
cns effects
dec: cmro2, cbf, icp cpp remains stable no analgesia
41
muscle side effect with etomidate
myoclonus- involuntary skeletal muscle contraction, dystonia or tremor likely due to imbalance between excitatory and inhibatory pathways of thalamocortical tract NOT a seizure
42
relationship between etomidate and seizures
no hx of seizures- no increased risk hx of seizures- can increase seizure like activity and possibly increase seizure risk
43
adrenocortical suppression and etomidate
cortisol and aldosterone synthesis are dependent on enzyme 11 beta hydrozylase (located in adrenal medulla) etomidate inhibits 11 beta hydrozylase and 17 alpha hydroxylase
44
how long does adrenocortical function suppression last with etomidate
5-8 hours (some say up to 24) no etomidate in sepsis pt!
45
2 subclasses of barbituates
thiobarbituates- sulfur molecule in 2nd position oxybarbituate- oxygen molecule in 2nd position
46
GABA a agonist
depresses reticular activating system in brainstem low/normal dose: increases affinity of gaba high dose: directly stimulates gaba a
47
onset and duration of thiopental
onset: 30-60 seconds duration: 5-10 mins
48
clearance of thiopental
liver (p450 enzymes) redistribution (not metabolism) determines awakening
49
what happens with repeated doses of thiopental
tissue accumulation-> prolonged wake up time-> hangover effect
50
cv effects of thiopental
-hypotension (venodiilation, dec preload, myocardial depression) -non immunogenic histamine release -baroreceptor preserrved- reflex tachycardia
51
resp effects of thiopental
-co2 curve shifted right (resp depression) -histamine-> bronchocontriction (caution if asthma!!)
52
cns effects of thiopental
decreased cmro2, cbf, icp, eeg
53
does thiopental have analgesia
no- low dose may increase perception of pain
54
acute intermittent porphyria
a defect in heme synthesis- promotes accumulation of heme precurosors (ALA induction) this type is most common and dangerous type
55
what drugs do you avoid with acute intermittent prophoryia
any drugs that induce ALA synthase barbs, etomidate, ketamine, toradol, amiodarone, ccb, birth control
56
tx for acute intermittent porphorya
-liberal hydration, glucose supplementation (reduces ALA synthase activity), heme arginagte, prevention of hypothermia
57
what happens if you inject thiopental intra arterial
tissue necrosis tx: phentolamine or phenoxybenzamine
58
gold standard for induction during ect
methohexital decreases seizure threshold- better quality seizure
59
induction dose of methohexital
1-1.5 mg/kg
60
MOA of precedex
alpha 2 agonist-> decreases camp-> inhibits locus coerulus in pons (sedation)
61
how does analgesia get produced by precedex
alpha 2 stim in dorsal horn of spinal cord (decreases glutamate and substance P release)
62
dose of precedex
loading: 1 mcg/kg over 10 min maintence: 0.4-0.7 mcg/kg/hr
63
onset and duration of precedex
onset 10-20 min duration 10-30 min (after d/c infusion)
64
clearance of precedex
liver (p450)
65
most common side effects of precedex
brady and hotn
66
rapid admin of precedex can cause
htn (alpha 2 stim) usually short lived
67
cns eeffects of dex
produces sedation resembling natural sleep (unique in this) -no reliable amnesia -pt arouses easily -dec cbf -no change in cmro2 -no change in icp
68
chemical make up of midazolam- how does this affect solubility
imidazole ring acidic ph- ring opens- increasing water solubility physiologic ph- ring closes- increasing lipid solubility
69
is midazolam water or lipid soluble in the vial
water needs no solvent like propylene glycol (diazepam and lorazepam need this)
70
MOA or midazolam
gaba a agonist- increases frequency of channel opening-> neuronal hyperpolarization most gaba a agonists increase channel open time but benzos increase open frequency
71
po dose in children for versed
0.5- 1 mg/kg
72
what is po bioavaliability of midazolam
po bioavaliability is 50% due to significant first pass metabolism
73
iv induction of versed dose
0.1-0.4 mg/kg
74
what induction agents produce an active metabolite
ketamine, versed, fospropofol
75
what agents have no active metabolites
precedex, propofol, etomidate
76
cv effects of versed (sedation vs induction)
sedation: minimal induction: dec svr and bp
77
cns effects of versed
sedation: minimal effects of cmro2 and cbf induction: decreases both
78
what agents can produce isoelectric eeg
propofol and barbs (versed cannot!)
79
does versed do analgesia
no
80
remimazolam
-ultra short acting benzo -vial needs to be protected from light -discard single use vial after 8 hrs
81
who is remimidazolam c/i in
pt with severe hypersensitivity rxn to dextran 40
82
benzo reversal
flumazenil (high affinity)
83
doa of flumazenil
30-60 min
84
dosing of flumazenil
0.2 mg IV (titrated in 0.1 mg increments q1 min)
85
potential side effects of flumazenil
does not increase sns tone, anxiety or neuroendocrine evidene of stress (narcan does!) but it can show signs of withdrawl including seizures
86